We have shown in preliminary studies in cattle that environmental cold (0 to -5C for 48 hours) produces a significant rise in pulmonary arterial pressure and vascular resistance. Other effects were reduction in ventilation and arterial oxygen tension and pH. This is new information which we have proposed should be documented and further studies undertaken to determine the basis of the pressor response. Our research has two major aims. One is to determine the nature and extent of interaction between hypoxia and cold on the pulmonary circulation. We particularly want to determine to what extent the cold pressor response is due to factors other than hypoxia and acidosis. Calves will be studied before and during cold exposure while breathing ambient air and air with increased and reduced oxygen to standardize arterial and alveolar PO2 and pH levels between control and cold. The second aim is to determine whether the sympathoadrenal system, prostaglandins and histamine are involved in the cold-induced pressor response. Catecholamine and prostaglandin assays, sympathetic blockade, tissue catecholamine depletion, inhibition of prostaglandin synthesis and adrenomedullary denervation are several techniques to be used. Results of our studies could be of major importance to human and animal health. If cold facilitates hypoxic pulmonary hypertension this could explain why the incidence of brisket disease in cattle is highest in the winter. Cold could also have adverse effects on humans who suffer from hypoxia. Asthmatics are known to have difficulty breathing in a cold environment.